Edi Catheter (NOT MRI SAFE)

Edi (Electrical activity of the diaphragm) catheters are nasogastric or orogastric catheters that estimate the neural respiratory drive and send that information to the mechanical ventilator. The ventilator uses that information to control respiration, guided by the patient's own neural control of breathing. This concept is called Neurally Adjusted Ventilatory Assist or NAVA).

The sensor part of the Edi Catheter is positioned in the esophagus at the level of the diaphragm (video on placement of the catheter). The Edi catheter from Maquete can also act as a normal nasogastric feeding tube and has a barium sulfate strip for identification on x-rays, but you wouldn't recognize it as anything other than a normal NG or OG tube unless you recognize that it looks different from the rest of the catheters used in your institution.

The above is kind of important because the catheter is NOT CONSIDERED SAFE FOR MRI.

References

Stein H, Hall R, Davis K, White DB. Electrical activity of the diaphragm (Edi) values and Edi catheter placement in non-ventilated preterm neonates. J Perinatol. 2013 Sep;33(9):707-11.

Dilated Cisterna Chyli: A Potential Mimicker of Lymphadenopathy

  

Axial (top) and coronal (bottom) contrast-enhanced CT images
demonstrate a retrocrural fluid-filled tubular structure with imperceptible walls
 (black arrows), the classic imaging features of a cisterna chyli

Coronal T2-weighted MRI shows the tubular cystic structure of the cisterna chili
and it's continuity with the thoracic duct (white arrow)

• The cistern chyli is a dilated lymphatic sac ommonly located in the right retrocrural region, at the level of L1-L2, extending 5-7 cm in CC dimension. It classically receives draining lymph from two lumbar trunks and an intestinal trunk, and continues cephalad as the thoracic duct

• Can enhance on delayed MRI >5 min

• Has an average size of 7.4 mm in the AP dimension, although some authors consider it dilated when ≥6 mm

• Dilatation can be secondary to lymphatic damage from prior gastroesophageal or retroperitoneal surgery, uncompensated cirrhosis, hypoalbuminemia, lymphangioleiomyomatosis, elevated central venous pressure, and biliary obstruction

• Size changes can vary depending on phase of respiration, hydration, and lower thoracic duct peristalsis

• Important to know of this entity because it can mimic retrocrural lymphadenopathy in the oncologic setting

• Mulitplanar reformations and MRI can help demontrsate the tubular cystic nature of the cistern chyli and its continuity with the thoracic duct 

References 

1. Rosenberger A, Abrams HL (1971) Radiology of the thoracic duct.Am J Roentgenol Radium Ther Nucl Med 111:807–820
2. Pinto PS, Sirlin CB, Andrade-Barreto OA, et al. (2004) Cisternachyli at routine abdominal MR imaging: a normal anatomicstructure in the retrocrural space. Radiographics 24(3):809–817 
3. Smith TR, Grigoropoulos J (2002) The cisterna chili: incidence and characteristics on CT. Clin Imaging 26:18–22
4. Arrive ́ L, Azizi L, Lewin M, et al. (2007) MR lymphography ofabdominal and retroperitoneal lymphatic vessels. AJR189(5):1051–1058
5. Gollub MJ, Castellino RA (1996) The cisterna chyli: a potentialmimic of retrocrural lymphadenopathy on CT scans. Radiology199(2):477–480 

Re

False Perpetuations: Main Portal Vein Size and Portal Hypertension

Perpetuation: A main portal vein (MPV) diameter >13 mm is "consistent with portal hypertension" (pHTN)

This cutoff of 13 mm is based on weak literature (mainly from the 1980's), some of which did not include comparison values of normal patients

• One comparative study using ultrasound found (Radiology 1982; 142: 167-172):
• In 79 patients with pHTN
• 36 had a MPV diameter of <13 mm 
• 33 had a MPV diameter >/= 13 mm
• The MPV was not visualized in 10 patients
• In the 45 control patients
• The MPV diameter was < 13 mm in 41 cases
• The MPV was not visualized in 4 patients. 

More recent studies have found that there is no significant difference in MPV diameters when comparing patients without cirrhosis to patients with cirrhosis, and the normal MPV diameter is significantly larger than the 13 mm cutoff

• A study (Eur J Gastroenterol Hepatol 2004; 16:147-155) from King's College using ultrasound (49 controls and 14 cirrhotics) found: 
• the average MPV diameters were 9.6 cm and 10.8 cm in patients without and with cirrhosis, respectively.
• A second study (JCAT 2008; 32: 198-203) from UCSF using CT (59 controls and 67 cirrhotics) found:
• The average MPV diameters were 14.5 cm and 14.8 cm in patients without and with cirrhosis, respectively.
• Using CT, the MPVs in healthy renal donor patients were measured before and after the administration of intravenous contrast, and in the axial and coronal planes (Abdom Radiol 2016; 41:1931-1936). This study found:
• The average MPV diameter was 15.5 +/- 1.9 mm
• This value was significantly different than 13 mm
• Post-contrast MPVs were 0.56 mm larger compared to non-contrast
• A positive correlation between BMI and height versus MPV diameter

In fact, the MPV size can be reduced in portal hypertension and has been described as a sign of hepatofugal MPV flow (AJR 2003; 181: 1629-1633). This study found:

• A MPV diameter of less than 1 cm is a highly sensitive (but not very specific) for MPV flow reversal in patients with cirrhosis

Systemic Mastocytosis

Systemic mastocytosis (SM) refers to mast cell infiltration in extra-cutaneous tissues. The symptoms of systemic mastocytosis are due to degranulation of mast cells and/or accumulation of mast cells in target organs.

Degranulation of mast cells

Symptoms can be caused by secretion of the following factors:

• Histamine: Pruritus, urticaria, hypotension, gastric hypersecretion, bronchoconstriction.
• Heparin: Local anticoagulation, osteoporosis
• Leukotrienes: Bronchoconstriction
• Prostaglandins: Bronchoconstriction, flushing
• Platelet-activating factor:
• Proteases:
• Tumor necrosis factor:

Accumulation of mast cells in organs

Accumulation of mast cells in organs can cause organ dysfunction. The so-called B findings refer to organ involvement without organ dysfunction. C findings refer organ involvement with organ dysfunction. The example above shows hepatic involvement with cirrhosis (white arrow) and ascites (yellow arrow) and nodal involvement with bulky adenopathy (red arrow). We also have involvement with diffuse sclerosis. Interestingly, the non-radiology literature stresses the more common osteoporosis, with scarce mention of the sclerosis that tends to dominate the radiology literature.

Diagnosis systemic mastocytosis

The diagnosis of SM requires either, 1 major and 1 minor OR 3 minor criteria. Warning: Boring for radiologists

The one major criterion is: Multifocal, dense infiltrates of mast cells (≥15 mast cells in aggregates) in sections of bone marrow and/or other extra-cutaneous organ(s).

Minor criteria are:

• Bone marrow or other extra-cutaneous organs: >25% of mast cells in the infiltrate are spindle-shaped or have atypical morphology, or of all mast cells in bone marrow aspirate smears, >25% are immature or atypical.
• Activating point mutation at codon 816 of KIT in bone marrow, blood, or another extra-cutaneous organ.
• Mast cells in bone marrow, blood, or other extracutaneous organs express CD2 and/or CD25 in addition to normal mast cell markers.
• Serum total tryptase persistently > 20 mg/mL (unless associated w clonal myeloid disorder).

Subtypes

• Indolent (ISM): No C findings
• Smoldering (SSM): 2+ B findings, no C findings
• Aggressive (ASM): C findings, no MCL features*
• Mast cell leukemia (MCL): BMBx diffuse infiltration by atypical, immature mast cells. Aspirate smears ≥20% mast cells.
• SM with associated hematologic neoplasm (SM-AHN): SM + MDS, MPN, AML, lymphoma, other

References

Akin C, Gotlib J. Systemic mastocytosis: Determining the subtype of disease. UpToDate

Management of Pancreatic Cystic Lesions

Thick slab MRCP image showing massive dilatation of the main pancreatic duct

Incidental cystic pancreatic lesions found on 13% of MRI abdomens

• Wide variety of pathology both benign and malignant
• Imaging findings and demographics are the key to diagnosis

Cystic Pancreatic Neoplasms (Four major categories)

1. Serous cystadenoma: Benign (very low malignant potential)
2. Mucinous cystic neoplasm (MCN): Premalignant or malignant
3. Intraductal papillary mucinous neoplasm (IPMN): Malignant potential (Main Duct >> Branch Duct)
4. Unusual cystic neoplasms:
   • Solid pseudopapillary neoplasm (SPN): Low grade malignancy
   • Cystic forms of more common neoplasms (neuroendocrine)

Nonneoplastic Pancreatic Cysts

• Pseudocyst
• Retention cyst
• Lymphoepithelial cyst
• Localized ductectasia

Major Imaging Features Guiding Management

• Number and size of cystic components: Risk of malignancy increases when size ≥ 3 cm
• Septations and solid components: Mural nodule has a 87% Sp and 56% Sn for malignancy
• Main pancreatic duct (MPD) dilatation and communication with the cystic lesion: MPD > 10 mm has a 77% Sp and 67-92% Sn for malignancy

Sendai Criteria

High Risk Stigmata

• Jaundice
• MPD ≥ 10 mm
• Enhancing solid component

Worrisome Features

• Size ≥ 3 cm
• MPD 5-9 mm
• Non-enhancing mural nodules
• Thick enhancing cystic wall
• Lymphadenopathy
• Abrupt Duct Termination

Management

• Any worrisome features present = Endoscopic Ultrasound (EUS) and Cyst aspiration with fluid analysis
• Any high risk stigmata present or suspicious cytology on EUS = Surgical resection
• MCN or SPN = Surgical resection
• Serous cystadenoma
  • 2-3 cm: F/U every 2 years
  • ≥ 4 cm: consider resection
• IPMN:
  • Main duct and combined type: Surgical resection (but depends on location, pt. age/clinical status)
  • Branch duct type = follow if < 3 cm and contains no solid components
    • If < 2cm F/U q1yr; if growth FU q6mo
    • If 2-3 cm F/U q6mo x 2 years, then q1yr
    • Consider EUS (if mucinous then resect)
    • If growth ≥ 3 cm, resect

What the Clinician/Surgeon wants to know

1. Number of cystic lesions
2. Largest cystic lesion
   • Unilocular
   • Multilocular: Microcystic (<2cm) or Macrocystic (> 2cm)
3. Lesion size
4. Lesion location: Head/Body/Tail
5. Septations: None/Thin/Thick (> 2mm)
6. Solid components: Present/Absent
7. Calcifications: None/Coarse/Rim/Central
8. Communication with MPD: Present/Absent
9. Main pancreatic duct diameter: > 5 mm/Not dilated

References

• Gandhi NS and Hecht E. “Adding Value to Clinical Care: Structured Reporting of Pancreatic Pathology”, Workshop Session Presentation, Society of Abdominal Radiology Annual Meeting, 2015
• Tanaka M,Fernández-del Castillo C, Adsay V,et al. International consensus guidelines 2012 for the management of IPMN andMCN of the pancreas. Pancreatology(2012) May-Jun;12(3):183-97
• DewhurstCE, Mortele KJ. Cystic tumors of the pancreas: Imaging and management. RadiolClin N Am 50(2012)467-86
• SahaniDV, Miller JC, and Fernandez C et al. Cystic pancreatic lesions: Classificationand Management. ACR (2009)
• SahaniDV, Kadavigere R, and Saoker A. Cystic Pancreatic Lesions: A SimpleImaging-based Classification System for Guiding Management. Radiographics (2005)25:1471-1484

Waldenström macroglobulinemia: Imaging Checklist

Waldenström macroglobulinemia (WM) is a lymphoplasmacytic lymphoma that is associated with an immunoglobulin M (IgM) monoclonal protein (M-protein). To establish the diagnosis of WM, it is necessary to demonstrate IgM monoclonal protein in the serum, along with histologic evidence of lymphoplasmacytic cells in the bone marrow. There is a similar spectrum of disease to that seen multiple myeloma (MGUS, smoldering myeloma, and frank myltiple myeloma) in WM: IgM monoclonal gammopathy of undetermined significance, smoldering macroglobulinemia, and WM.

WM is more common in men and in whites. The most common presenting symptom is fatigue related to a normochromic or normocytic anemia. Patients can also have peripheral neuropathy. Hyperviscosity syndrome, which includes epistaxis, gingival bleeding, and retinal hemorrhage is related to high plasma IgM concentrations and is becoming less common due to earlier diagnosis. It is rarely seen in patients with IgM concentration of <4,000 mg/dL.

The checklist for reviewing images in these patients includes clinical features, complications of the disease, and potential mimickers. These include:

• Lymph nodes: The majority of patients have adenopathy on FDG-PET and CT.
• Bone marrow: Almost half of patients show diffuse increased uptake on PET, and about 90% will show marrow signal changes on MRI (diffuse in more than half). This can be due to marrow infiltration or hyperplasia due to anemia.
• Spleen size: Between 10-20% of patients will have splenomegaly on imaging
• Liver size: Hepatomegaly can be seen in patients, but the prevalence on imaging has not been reported.
• Viscera: Between 10-20% of patients will have visceral or extra-nodal sites of involvement on imaging.
• Venous patency: To assess for thrombosis due to hyperviscosity from high IgM protein
• Vessel walls: To assess for immune complex vasculitis due to IgM protein
• Presence of hemorrhage: Due to low levels of von Willebrand factor
• Central nervous system: To assess for presence of Bing-Neel syndrome, which is perivascular infiltration of small lymphocytes, lymphoplasmacytoid cells, and plasma cells in the brain parenchyma and/or spine.
• Amyloidosis: Imaging features of amyloidosis should be sought, since it can also present with an IgM monoclonal protein and neuropathy (particularly if the light-chain isotype is lambda).

WM can be difficult to differentiate from marginal zone lymphoma. MYD88 mutation L265P is more commonly seen in WM (67% of cases), and less commonly in splenic marginal zone lymphoma (4%) and mucosa-associated lymphatic tissue lymphoma (7%).

Because the M-protein of patients with WM is almost always IgM, a broad differential should be considered for lucent bone lesions (the M-protein of multiple myeloma is usually IgG, followed by IgA and IgD, with IgM myeloma making up about 1% of cases). The same can be said for sclerotic bone lesions with or without peripheral neuropathy (the M-protein of POEMS is usually IgG and IgA, with IgM POEMS being very rare). However, this information is not always available when interpreting initial staging studies for patients with newly diagnosed plasma cell dyscrasia.

References

• Banwait R, O'Regan K, Campigotto F, Harris B, Yarar D, Bagshaw M, Leleu X, Leduc R, Ramaiya N, Weller E, Ghobrial IM. The role of 18F-FDG PET/CT imaging in Waldenstrom macroglobulinemia. Am J Hematol. 2011 Jul;86(7):567-72.
• Gertz MA. Waldenström macroglobulinemia: 2013 update on diagnosis, risk stratification, and management. Am J Hematol. 2013 Aug;88(8):703-11.
• Moulopoulos LA, Dimopoulos MA, Varma DG, Manning JT, Johnston DA, Leeds NE, Libshitz HI. Waldenström macroglobulinemia: MR imaging of the spine and CT of the abdomen and pelvis. Radiology. 1993 Sep;188(3):669-73.

Splenic Abscess

The CECT images above are from a patient who underwent sleeve gastrectomy (blue arrow) and experienced worsening abdominal pain in the weeks that followed. She was admitted with sepsis. There are necrotic areas within the spleen and multiple rim enhancing collections of air and fluid (red arrows) compatible with abscesses. Left upper quadrant fluid collections (sterile and infected) are a known complication of bariatric surgery.

REFERENCES

Blachar A and Federle MP. Gastrointestinal complications of Roux-en-Y gastric bypass surgery in patients who are morbidly obese: findings on radiography and CT. AJR Am J Roentgenol 2002;179:1437-42.

Yu J, Turner MA, Cho SR, et al. Normal anatomy and complications after gastric bypass surgery: helical CT findings. Radiology 2004;231:753-60.

Necrotizing Pancreatitis

Necrotizing pancreatitis is perhaps the most severe complication of acute pancreatitis because of the high associated mortality rate.  Bacterial contamination of pancreatic necrosis carries a 40-70% mortality rate, even after surgical debridement. Thus, early detection of necrosis is crucial in patient management. 

CECT will show lack of enhancement of the necrotic regions.  This finding is usually accompanied by other imaging indicators of pancreatitis such as infiltration of the peripancreatic fat planes. T2W MRI will show increased signal intensity of the necrotic regions while T1W post contrast images will show nonenhancing areas with decreased signal intensity. 

The above CECT images are from a young male admitted with acute pancreatitis whose clinical status was worsening. Lack of enhancement of the distal pancreatic body and tail are seen (red arrow)  consistent with necrosis. Note, the normal enhancement of the pancreatic head (blue arrow).

REFERENCES
Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002;23:603-13.
O'Connor OJ, Buckley JM, Maher MM. Imaging of the complications of acute pancreatitis. AJR Am J Roentgenol 2011;197:W375-81.

Focal Nodular Hyperplasia in the Caudate Lobe

Incidentally seen on a trauma CECT was a hyperdense with central low attenuation in the caudate lobe (first image). Further work up with MR re-identified the mass as isointense on T1WI, isointense with a hyperintense central scar on T2WI, and enhancement of the central scar on post contrast T1WI.  The findings are compatible with focal nodular hyperplasia.

Post Bulbar Duodenal Ulcer

The above images from a double contrast upper GI study show a filling defect in the post bulbar duodenum with radiating folds (arrow) causing distal narrowing/stricture most consistent with a post bulbar ulcer.

Post bulbar ulcers are rare and constitute about 5% of all duodenal ulcers. There is a higher likelihood of life threatening bleeding with post bulbar ulcers than with ulcers in the first portion of the duodenum. While ulcers of the duodenal bulb are almost always associated with H. pylori infection, the prevalence of H. pylori in post bulbar ulcers is significantly less and post bulbar ulcers should be worked up for malignancy and Zollinger-Ellison syndrome. 


REFERENCES
Carucci LR, Levine MS, Rubesin SE, Laufer I. Upper gastrointestinal tract barium examination of postbulbar duodenal ulcers. AJR Am J Roentgenol 2004;182(4):927-30.
Kaufman SA and Levene G. Postbulbar duodenal ulcer. Radiology 1957;69:848-52.

Intestinal Angioedema

Angioedema is a noninflammatory disease characterized by increased capillary permeability with extravasation of intravascular contents leading to edema. The face, limbs, and airways may be involved and angioedema of the latter can cause life threatening airway obstruction. Intestinal involvement is also reported and can present with acute abdomen, or in rare cases, hypovolemic shock.

Angioedema is due to hereditary and idiopathic, or secondary to therapy with angiotensin converting enzyme (ACE) inhibitors in patients with hypertension.

CECT findings include bowel wall and mucosal thickening, enhancement of the mucosa (differentiates from ischemic bowel wall thickening), prominent mesenteric vessels, and ascites. 


REFERENCES
De Backer AI, De Schepper AM, Vandevenne JE, et al. CT of angioedema of the small bowel. AJR Am J Roentgenol 2001;176(3):649-52.
Scheirey CD, Scholz FJ, Shortsleeve MJ, et al. Angiotensin-converting enzyme inhibitor-induced small-bowel angioedema: clinical and imaging findings in 20 patients. AJR Am J Roentgenol 2011;197(2):393-8.

Causes of Hepatic Capsular Retraction

Peripheral Cholangiocarcinoma

• malignant tumor arising from interlobular bile ducts
• peripheral enhancement on arterial phase CECT with gradual centripetal fill in
• delayed enhancement is common due to fibrotic regions within mass
• may have dilated bile ducts upstream from the lesion

Confluent Hepatic Fibrosis

• occurs in the setting of cirrhosis
• usually in the medial segment of the left lobe and/or anterior segment of the right lobe
• peripheral wedge shaped regions of low attenuation on CECT that show delayed enhancement
• biliary ductal dilatation not seen

Metastases

• treated adenocarcinoma (usually colorectal, breast) can cause hepatic capsular retraction 
• regions of fibrosis (pseudo-cirrhosis) may also be seen

REFERENCES

Fennessy FM, Moretele KJ, Kluckert T, et al. Hepatic capsular retraction in metastatic carcinoma of the breast occurring with increase or decrease in size of subjacent metastasis. AJR Am J Roentgenol 2004;182(3):651-5.

Lee JW, Kim S, Kwack SW, et al. Hepatic capsular and subcapsular pathologic conditions: demonstration with CT and MR imaging. Radiographics 2008;28:1307-23.

Lipson JA, Qayyum A, Avrin DE, et al. CT and MRI of hepatic contour abnormalities. AJR Am J Roentgenol 2005;184(1):75-81.

Achalasia

Achalasia is a disorder of esophageal dysmotility due to failure of the gastroesophageal sphincter to relax because of destruction of its myenteric plexus. Primary achalasia is considered idiopathic while secondary achalasia could be due to destruction of the myenteric plexus by tumor or infection (Chagas disease). The radiologic diagnosis of primary achalasia is best made with barium studies which will show marked dilation of the esophagus with smooth narrowing near the GE junction (bird's beak deformity). Real time imaging will also show absent primary peristalsis and the presence of tertiary contractions. While cross sectional imaging is not the most sensitive in diagnosing achalasia, sometimes the finding is made incidentally as in the above case. The differential diagnosis of achalasia was previously discussed here.


REFERENCES
Noh MH, Fishman EK, Forastiere AA, et al. CT of the esophagus: spectrum of disease with emphasis on esophageal carcinoma. Radiographics 1995;15:1113-34.
Woodfield CA, Levine MS, Rubesin SE, et al. Diagnosis of primary versus secondary achalasia: reassessment of clinical and radiographic criteria. AJR Am J Roentgenol 2000;175(3):727-31.

Killian Jamieson Diverticulum

Killian is usually mentioned when discussing the Killian's dehiscence which is the gap in the posterior hypopharynx where the muscle fibers of the cricopharyngeus muscle and inferior constrictor muscle diverge. This site is where Zenker's diverticula occur.

The Killian-Jamieson space is below the cricopharyngeus muscle and lateral to the longitudinal muscle of the esophagus. This muscular gap is the location of the rarer Killian-Jamieson diverticulum. Fluoroscopy will show an outpouching along the anterolateral esophagus inferior to the cricopharyngeus muscle (as opposed to along the posterior esophagus and superior to the cricopharyngeus muscle in the case of a Zenker's diverticulum). 

REFERENCES

Rubesin SE and Levine MS. Killian-Jamieson diverticula. AJR Am J Roentgenol 2001;177:85-9.

Gossypiboma

Stemming from the Latin gossypium, meaning cotton, gossypiboma refers to retained cotton products such as surgical sponges. A gossypiboma can elicit an inflammatory response leading to formation of an intraabdominal abscess, or cause obstructive symptoms due to mass effect.


REFERENCES
Manzella A, Filho PB, Albuquerque E, et al. Imaging of gossypibomas: pictorial review. AJR Am J Roentgenol 2009;193:S94-101.

Endovascular Management of TIPS-related Hepatic Encephalopathy

Hepatic encephalopathy is a common complication that occurs after creation of a TIPS shunt. It is typically managed conservatively with modifications in diet and medication. In patients who do not respond to conservative management, liver transplantation may be an option. Some endovascular techniques aimed at reducing the amount of blood shunted away from the liver may also be employed.

• shunt occlusion via embolic agents
• has risk of variceal rebleeding
• sudden changes in hemodynamics (cardiac output, hypotension, metabolic acidosis) can be fatal
• reversible shunt occlusion using short term balloon occlusion of the TIPS can prevent complications from variceal rebleeding (occlusive balloon can be deflated if life threatening bleeding occurs and thus TIPS can be reopened)
• shunt reduction
• using constrained stents to reduce the lumen of the shunt
• makes it difficult to regulate blood flow through the shunt, especially around the constrained portions
• adjunct embolization of the dead space around the shunt can be performed
• use of constrained covered stent grafts has allowed better control of flow through the shunt while reducing its lumen
• retrograde embolization of a splenorenal shunt with ethanolamine oleate
• can only be done when a spontaneous splenorenal shunt is present
• maintains patency of TIPS
• severe renal dysfunction and pulmonary edema are among some of the side effects of ethanolamine usage

REFERENCES

Madoff DC, Wallace MJ, Ahrar K, et al. TIPS-related hepatic encephalopathy: management options with novel endovascular techniques. Radiographics 2004;24:21-36.

Mesenteric Hematoma Revisited

The above CECT images show hazy stranding of the mesentery in a patient with blunt abdominal trauma. Findings are consistent with a mesenteric hematoma, previously discussed here.

Imaging the Pancreas

Pancreatic adenocarcinoma carries a poor prognosis. CT is a fine modality for imaging the pancreas and determining the nonresectability of a mass. Pancreatic imaging protocols tend to be biphasic with image acquisition performed in the pancreatic parenchymal and portal venous phases. The pancreatic parenchymal phase involves a scanning delay of 40-70 seconds while the portal venous phase is imaged at a delay of 60-70 seconds. Arterial phase imaging should be reserved for patients requiring CT angiography to evaluate for tumor resectability.


REFERENCES
McNulty NJ, Francis IR, Platt JF, et al. Multi-detector row helical CT of the pancreas: effect of contrast enhanced multiphasic imaging on enhancement of the pancreas, peripancreatic vasculature, and pancreatic adenocarcinoma. Radiology 2001;220:97-102.

The Flat Cava Sign Revisited

Recently discussed here, these images show a flattened IVC (better seen on second image, red arrow) in a patient with ischemic small bowel. 

SMA syndrome

Superior mesenteric artery syndrome (SMA syndrome) refers to compression of the third portion of the duodenum between the aorta and SMA. The images above show classic CECT findings: there is dilation of the stomach, first and second portions of the duodenum (first image), with narrowing of the duodenum as it crosses the spine (second image) and collapse of the distal duodenum (third image).


REFERENCES
Agrawal GA, Johnson PT, Fishman EK. Multidetector row CT of superior mesenteric artery syndrome. J Clin Gastroenterol 2007;41(1):62-5.